Fig. 1.  Schematic representation of stress hyperglycemia. (A ) In stress conditions, tissues that absorb glucose under the influence of insulin (insulin-mediated glucose uptake [IMGU]) become resistant to the effects of insulin (peripheral insulin resistance). Consequently, glucose is diverted away from IMGU tissues, and neoglucogenic substrates (i.e. , alanine, glycerol, and lactate) are released and used by the liver to produce glucose. (B ) In the liver, endogenous glucose production is fueled by glycogenolysis and neoglucogenesis, both stimulated by the counterregulatory hormones and less inhibitable by circulating glucose (central insulin resistance). (C ) The resulting hyperglycemia finally leads to increased non–insulin-mediated glucose uptake (NIMGU) tissues, under the influence of proinflammatory cytokines. EGP = endogenous glucose production; GLUT = glucose transporters; IL = interleukin; TNF = tumor necrosis factor.

Fig. 1.  Schematic representation of stress hyperglycemia. (A ) In stress conditions, tissues that absorb glucose under the influence of insulin (insulin-mediated glucose uptake [IMGU]) become resistant to the effects of insulin (peripheral insulin resistance). Consequently, glucose is diverted away from IMGU tissues, and neoglucogenic substrates (i.e. , alanine, glycerol, and lactate) are released and used by the liver to produce glucose. (B ) In the liver, endogenous glucose production is fueled by glycogenolysis and neoglucogenesis, both stimulated by the counterregulatory hormones and less inhibitable by circulating glucose (central insulin resistance). (C ) The resulting hyperglycemia finally leads to increased non–insulin-mediated glucose uptake (NIMGU) tissues, under the influence of proinflammatory cytokines. EGP = endogenous glucose production; GLUT = glucose transporters; IL = interleukin; TNF = tumor necrosis factor.

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